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线粒体损伤与衰竭之路。

Mitochondrial Damage and the Road to Exhaustion.

机构信息

Suzhou Institute of Systems Medicine, Suzhou, Jiangsu 215123, China; Center for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, 100005 Beijing, China.

Suzhou Institute of Systems Medicine, Suzhou, Jiangsu 215123, China; Center for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, 100005 Beijing, China; Key Laboratory of Synthetic Biology Regulatory Element, Chinese Academy of Medical Sciences, Beijing, China.

出版信息

Cell Metab. 2020 Dec 1;32(6):905-907. doi: 10.1016/j.cmet.2020.11.004.

Abstract

Two recent studies published in Nature Immunology map out the link between dysregulated mitochondrial metabolism and terminal exhaustion of tumor-infiltrating T lymphocytes. Yu et al. (2020) and Vardhana et al. (2020) show that defective mitophagy or impaired oxidative phosphorylation triggers mitochondrial reactive oxygen species production, which in turn promotes a T cell exhaustion program, limiting T cell proliferation and self-renewal.

摘要

两篇最近发表在《自然免疫学》上的研究阐明了失调的线粒体代谢与肿瘤浸润 T 淋巴细胞终末耗竭之间的联系。Yu 等人(2020 年)和 Vardhana 等人(2020 年)表明,有缺陷的线粒体自噬或氧化磷酸化受损会触发线粒体活性氧的产生,进而促进 T 细胞耗竭程序,限制 T 细胞的增殖和自我更新。

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